Probable Electrocution in a Quarter Horse Stallion
Stephanie D Janeczko
Advisors: Dr. Monica Figueiredo and Dr. Julia Flaminio Clinicians: Dr. Monica Figueiredo and Dr. Julia Flaminio
Senior Seminar Paper Cornell University College of Veterinary Medicine
March 31, 2004
Key words: electrocution, ventricular tachycardia

Probable Electrocution in a Quarter Horse Stallion
Stephanie Janeczko, Monica Figueiredo, Julia Flaminio
Abstract. Although electrocution is widely reported in the human literature, there are no welldocumented cases reported in horses. A probable diagnosis of electric shock injury was made in the case of an 18 year old Quarter Horse breeding stallion that presented to the Cornell University Hospital for Animals with a chief complaint of seizure-like activity following loss of electrical power at the farm. Pertinent physical exam findings included hyperhidrosis, diffuse muscle fasciculations and contractions, and severe ataxia involving all four limbs. A complete blood count revealed a marked leukocytosis, characterized by a neutrophilia and eosinophilia. The neurologic signs resolved within 18 hours of presentation with minimal therapeutic intervention. Ventricular tachycardia without associated clinical signs developed 20 hours following presentation, and resolved without treatment. The rapid and complete recovery made an infectious process or structural lesion highly unlikely, leading to a presumptive diagnosis of electrocution.
Introduction. Electric shock is responsible for hundreds to thousands of injuries to both people and animals each year1, and the injuries can be divided into those caused by lightning strike and
those caused by electrocution. Lightning strike injuries are frequently reported in both the
human and veterinary literature, and have been divided into at least four types: direct strike, side
flash, stride potential, and flash-over phenomenon, as determined by the pathway of the current.
Electrocution, on the other hand, is common in people, particularly children and construction
workers, but has not been documented in horses aside from a few anecdotal reports.
Electrical current is converted to thermal energy and causes direct damage to tissues, with
the degree of damage being determined by the resistance of the tissues it comes in contact with
and by the intensity of the current.. Nerves and blood vessels offer the least resistance due to
their high water content and conductive properties, while structures like bone, fat, and tendons have a higher resistance1. Accordingly, lower resistance structures act to conduct the current
while high resistance tissue are more likely to convert the current to thermal energy and
coagulate. Electrical current also leads to indirect injury by causing severe muscle contractions.
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In addition, the severity of the injury depends on the intensity of the current, which is a factor of both voltage and resistance, as well as the pathway through the body and the duration of current with the electrical source. Any organ system can be affected, and clinical signs vary widely depending on the precise details of the variables previously mentioned. Some of the more common injuries reported in both the human and veterinary literature include myocardial necrosis, arrhythmias, cutaneous burns, and CNS signs1. However, many other lesions have been reported, such as traumatic rupture of the tympanic membrane and cataracts that form months to years after a lightning strike. Death is, unfortunately, not uncommon, and is usually a result of either respiratory arrest or ventricular fibrillation. In cases of electrocution by direct current, the massive shock depolarizes the entire myocardium and may result in asystole. Treatment is symptomatic and varies with the nature of the clinical signs.
Clinical signs, however, seem to vary from species to species and with the specific type of electrical injury. It is well known that young companion animals can be electrocuted by chewing on household wires, which would result in a low voltage alternating current. Clinical signs in such cases include oral burns, dyspnea, pulmonary edema, and emesis. There are several reports of swine that have been electrocuted through faulty wiring on the farm2,3, and the predominant clinical sign noted was posterior paresis resulting from vertebral and pelvic fractures. Stray voltage has been proposed as a potential cause of behavioral changes and production losses in dairy cows4. Many cases of lightning strike injuries have been reported in animals, with clinical signs ranging from very mild symptoms to death. Compared to the number and detail of reports in the human literature relating to electric shock injuries, the veterinary literature is incomplete. Coupled with the range of clinical signs attributable to
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electrical injury, this makes it exceedingly difficult to arrive at a definitive diagnosis of electric shock injury.
Case History and Chief Complaint. Buckskin Cody, an 18 year old Quarter Horse breeding stallion, presented to the Cornell University Hospital for Animals (CUHA) with a chief complaint of seizure-like activity. Cody had been fed and turned out in his usual paddock earlier that morning and appeared to be normal. Several hours later, the owner noted the stallion to be rolling in his paddock but described that as normal behavior. Shortly after, however, she saw him to have a stiff gait and muscle contractions. Cody was extremely anxious and had what the owner described as seizure-like activity: he would stumble and paddle or kick with his forelimbs, trying to climb on the owner. The owner had also reported that the horse never went down in lateral recumbency. The owner administered 20ml of flunixin meglumine (Banamine; ScheringPlough, Kenilworth, NJ) intramuscularly and immediately brought Cody to CUHA for a complete evaluation.
As per the history obtained from the owner, Cody was up to date on all vaccines, including tetanus, influenza, West Nile virus, equine protozoal myelitis (EPM), and rabies. He was also on a regular, vigorous deworming program. No new animals had been introduced to the farm and there were no other similarly affected animals on the premises. Cody’s diet had not been changed. He had no known access to toxins. Cody did not have any history of colic or exertional rhabdomyolosis (“tying up”). Although he had never been tested for the HYPP gene, the stallion Impressive was not in Cody’s lineage and he had never before exhibited clinical signs consistent with hyperkalemic periodic paralysis.
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Cody’s medical history is unremarkable. He had previously sustained a mild injury to his left forelimb that resulted in a slight lameness incompatible with his presenting ataxia. The owner reported that there had been a wind storm that morning, and the farm had lost power about the same time that she noted Cody’s abnormal behavior.
Physical Examination Findings. The patient presented for evaluation was an adult Quarter Horse stallion in good body condition. He was extremely agitated and unwilling to stand in one place for any length of time. Spontaneous muscle fasciculations and intermittent abdominal muscle contractions were noted at rest. Hyperhidrosis was noted, despite euthermia. When walked, the stallion was extremely ataxic in all four limbs (grade 4/5) and would drift to the left. He exhibited a stiff, hypermetric gait involved all four limbs that was slightly worse on the left compared with the right. Proprioceptive deficits were worse when circled to the left compared with circling to the right. Examination of cranial nerves was unremarkable. Thoracic auscultation was incomplete because of the severe ataxia and constant muscle fasciculations. Gut sounds and manure were within normal limits. No cutaneous lesions were noted.
Problem list. Following physical examination, the problem list included: hyperhidrosis ataxia; upper motor neuron/general proprioceptive deficits (cervical vertebrae C1-C6 lesion, left worse than right); spontaneous muscle fasciculations and contractions. Further examination and diagnostics later uncovered additional problems: leukocytosis, neutrophilia with a left shift, eosinophilia, elevated creatinine kinase levels, asymptomatic ventricular tachycardia, and positive Equine Protozoal Myelitis (EPM) western blot.
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Differential diagnoses. At the time of presentation, the list of differentials included infectious processes, structural lesions, and toxic/metabolic causes. Infectious processes thought to be a cause of clinical signs were West Nile virus, Equine Eastern Encephalitis virus, rabies, EPM, or aberrant parasitic migration. A structural cervical lesion, such as arthritis, fracture, an abscess, or neoplasia was also considered. Hepatic encephalopathy and a toxic insult, as well as electrocution, were also considered as possibilities.
Initial Work-up and Laboratory Data. Peripheral blood was submitted for a complete cell count (CBC), chemistry panel, EPM western blot, and West Nile serology. A fecal sample was submitted for parasite analysis by floatation. An examination was also performed by our neurologist.
The initial CBC revealed a leukocytosis characterized by a neutrophilia with a left shift and eosinophilia (WBC 20,700/uL, Seg N 16,600/uL, Band N 400/uL, Eosin 1,000/uL). Pertinent abnormalities on the chemistry panel included mildly elevated creatine kinase (2315 U/L) and alkaline phosphatase (478 U/L) levels. No parasites were detected on fecal floatation. West Nile virus serum neutralization antibodies and IgM capture ELISA were both negative. Western blot of the serum was weakly positive for EPM.
A limited neurologic examination was consistent with a left sided lesion affecting the upper motor neurons and general proprioceptive pathways to all four limbs. The anatomical diagnosis was pons to C6.
Treatment. Cody was started on symptomatic supportive therapy and placed in a padded stall to prevent self-inflicted injury. Intravenous fluids (Plasmalyte A) with 500mL DMSO (1g/kg BW,
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10% solution, q12 hours) were started as treatment for possible cerebral edema or central nervous system (CNS) damage. Vitamin E (10,000 IU PO q24 hours) and thiamine (5g IV q24 hours) were also administered for their antioxidant properties. Additionally, thiamine has a neuroprotective quality that was desirable in this case. Ponazuril, an antiprotozoal paste, was administered (1000# dose q24 hours) as therapy for potential EPM. Hay and water were available ad libitum. Naxcel (1g IV q12 hours) was added for its broad spectrum bactericidal activity after the left shift was identified on the CBC.
Outcome. The following morning, less than 18 hours after presentation, no neurologic abnormalities were detectable. Physical examination, including thoracic and abdominal auscultation, was within normal limits. The neurologist failed to identify any appreciable neurologic deficits at that time, although the stallion did appear to have a slight lameness in the left forelimb.
On that morning, a rapid, irregular heart beat was ausculted. An ECG was immediately performed, and was consistent with sustained ventricular tachycardia (110-120bpm). The lead I ECG showed negative QRS complexes and no P waves. The lead III ECG had identifiable P waves, but they were not associated with the QRS complexes. Because Cody’s attitude, pulse strength, and mucus membrane color remained within normal limits, treatment was not initiated and he was closely observed for the remainder of the day. Additional ECG tracings performed throughout the day repeatedly showed a sustained ventricular tachycardia, although the resting heart rate gradually decreased. The Cardiology service was consulted and examined Cody the following morning. A six lead ECG at that time revealed a normal sinus rhythm and no abnormalities were detected.
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The stallion was also sedated with xylazine (100mg IV) for a lumbosacral cerebrospinal fluid (CSF) tap. Cerebrospinal fluid was submitted for cytology and an EPM Western blot. Cody was continued on symptomatic treatments described previously and observed closely for another 24 hours. He was discharged to his owner approximately 96 hours after presentation with no clinical signs.
Discussion. At the time of discharge, Cody’s chemistry values were within normal limits and hematological abnormalities were resolving. Both the segmented and banded neutrophil counts were within the normal range, and although the eosinophils were still elevated they had showed a trend towards normal. CSF cytology was unremarkable. Although the serum and CSF showed a weak positive result for EPM, this was attributed to exposure to Sarcocystis neurona rather than actual infection. His rapid recovery with minimal treatment and without further complication made an infectious process highly unlikely. Likewise, a structural cervical lesion such as a fracture, abscess, or neoplasia was highly unlikely to have caused the clinical signs shown on presentation. Nevertheless, further diagnostics such as a CT scan or cervical radiographs were offered to the client but not performed. The acute onset of multisystemic signs coupled with a rapid recovery led to a presumptive diagnosis of electric shock injury.
Clinical signs of electric shock injury vary with the intensity of the current, pathway through the body, and species affected. These injuries should be viewed and managed as a multisystemic injury. Any tissue can be affected, but the most common clinical signs reported in people include arrhythmias, cutaneous burns, neurologic deficits (including seizures), respiratory arrest, and severe muscle contractions5. As in people, treatment is purely supportive. Adding to the difficulty of treatment is the fact that animals seem to be more susceptible than
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humans to the effects of electric shock. Indeed, it is reported that the majority of people struck by lightning survive while the majority of horses do not5,6.
Horses are considered to be more susceptible to electrical injury for several reasons. There are many anecdotal reports where horses have fallen down, presumably due to electrical shock, but their riders were unaffected. Similarly, there are reports of stray voltage having clinical affects on cattle while the people on the farm felt nothing unusual. Horses have twice the ground contact (4 feet vs. 2 feet) that people do and are frequently wearing horseshoes which may serve to better conduct current, although the latter statement has not been proven. Certainly they are unlikely to be wearing insulating rubber soled shoes like people do. Furthermore, horses’ feet are more likely to be wet, which drastically decreases the inherent resistance of the skin, which is the main resistance the body has to electrical current. Heat is easily dissipated from wet skin, leading to better conduction and less injury, and this may explain why only about 30% of animal cases reported note cutaneous burns. The circuit is closed through the trunk in horses (resulting in a pathway that involves the heart), while in people it may be closed only through the lower half of the body. Perhaps most importantly, however, horses’ limbs are considerably farther apart than people’s. Stride potential, one of the many factors that determines that severity of injury, is determined by Ohm’s law: V=IR, where V=voltage, I=current, and R=resistance. The value of R is partially determined by the distance between the points (i.e. the feet) to which the voltage is applied; the greater the value of R, the greater the voltage7.
In this case, the patient had an acute onset of neurologic signs, delayed development of ventricular tachycardia, and a marked leukocytosis, all of which resolved with minimal to no
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intervention. All other differentials were ruled out either on the basis of negative laboratory results or due to the complete and rapid recovery with minimal treatment.
Any type of neurologic damage is possible with electrical injuries and can appear at any time. In people, those deficits that occur immediately following the injury are more likely to resolve than those that appear hours or days later. Ataxia and vestibular signs have been reported in two horses following a suspected lightning strike8. Loss of consciousness has been reported in cats and dogs. Frequently, the actual cause or type of injury is not identified and any degree of resolution is possible.
Arrythmias are extremely common with a reported incidence ranging from 10-46%9. Longer contact with the current makes an arrhythmia more likely to develop due to the greater chance that a shock will fall during the vulnerable period of the cardiac; however, it appears that any electrical injury can produce an arrhythmia10. The most common ECG abnormalities noted in people include sinus tachycardia, S-T and T-wave changes, and ventricular fibrillation. Although most occur immediately after the electrical injury, delayed ventricular tachycardia has been reported in at least three people following lightning strike11; some cases resolved spontaneously without therapy.
Electrocution is known to cause leukocytosis in people. Rey and Wolf reported a case of an electrical accident that resulted in the development of a striking leukocytosis with neutrophilia, eosinopenia, and lymphopenia, seemingly as a stress reaction12. Eosinophilia has not been documented to result from electrocution in any species. The main differential diagnoses of eosinophilia in horses, which includes cutaneous habronemiasis, lymphoma, and rarely internal parasitism, were highly unlikely in this case.
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In conclusion, the stallion presented with an acute onset of severe neurologic signs, delayed development of ventricular tachycardia, and a leukocytosis. Initial differential diagnoses at the time of initial examination were rabies, West Nile virus, Eastern Encephalitis, EPM, a cervical lesion, aberrant parasitic migration, toxic insult, or electrocution. The rapid recovery with minimal therapy made an infectious cause or a structural lesion highly unlikely, leading to a presumptive diagnosis of electrocution.
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References:
1. Koumbourlis, AC. Electrical injuries. Crit Care Med 2002;30(11):S424-S430. 2. Steffen DJ, Schoneweis DA, Nelssen JL. Hind limb paralysis from electrical shock in
three gilts. JAVMA 1992;200(6):812-813 3. Giles N and Simmons JR. Electrocution of pigs. Vet Rec 1975;97:305-306. 4. Smith CA. Stray voltage: real problem or red herring? JAVMA 1994;204(9):1341-1346. 5. Craig SR. When lightning strikes: pathophysiology and treatment of lightning injuries.
Postgrad Med 1986;79(4):109-112, 121-124. 6. Williams MA. Lightning strike in horses. Compendium 2000;22(9):860-866. 7. NovalesM, Hernandez E, Lucena R. Electrocution in the horse. Vet Rec 1998;142:68. 8. Bedenice D, Hoffman AM, Parrott B, et al. Vestibular signs associated with suspected
lightning strike in two horses. Vet Rec 2001;149:519-522. 9. O’Conor CE. Management of electrical injury in the emergency department. Ir Med J
2003;96(5):133-134. 10. Forrest FC, Saunders PR, McSwinney M, et al. Cardiac injury and electrocution. J R
Soc Med 1992;85:642-643. 11. Jensen PJ, Thomsen PEB, Bagger JP, et al. Electrical injury causing ventricular
arrhythmias. Br Heart J 1987;57:279-283. 12. Rey JJ and Wolf PL. Extreme leucocytosis in accidental electric shock. Lancet
1968;1(7532):18-19.
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